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Updated: Jun 27, 2026

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

Decrease in macrolide resistance and clonal instability among Streptococcus pyogenes in Portugal.

C Silva-Costa¹, F R Pinto, M Ramirez

¹Institute of Microbiology/Molecular Medicine, Faculty of Medicine, Lisbon University, Lisbon, Portugal.

Clinical Microbiology and Infection : the Official Publication of the European Society of Clinical Microbiology and Infectious Diseases

|December 3, 2008

Summary

This summary is machine-generated.

Macrolide resistance in Streptococcus pyogenes shifted from M to MLS(B) phenotypes between 1998-2003, then reversed by 2004-2006 due to decreased M phenotype prevalence. Clonal dynamics, not just antibiotic use, influence resistance patterns.

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Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

Area of Science:

Microbiology
Molecular Biology
Epidemiology

Background:

Macrolide resistance in Streptococcus pyogenes (group A streptococci) showed stable trends from 1998-2003.
A significant shift in dominant resistance phenotypes (MLS(B) decreasing, M increasing) occurred during this period.

Purpose of the Study:

To characterize macrolide resistance trends in Streptococcus pyogenes from 2004-2006.
To investigate the clonal dynamics and genetic basis of macrolide resistance in Portugal.

Main Methods:

emm typing
T serotyping
Pulsed-field gel electrophoresis (PFGE) profiling
Multilocus sequence typing (MLST)

Main Results:

Erythromycin resistance declined from 2004-2006 due to a decrease in the M phenotype, while the MLS(B) phenotype remained stable.
Characterization revealed a diverse population with both previously identified and novel PFGE clusters.
Specific clones showed shifts in associated resistance genes, e.g., T12/emm12/ST36 predominantly associated with erm(B) instead of mef(A).

Conclusions:

Macrolide resistance patterns in Streptococcus pyogenes are not static and showed instability between 2004-2006.
Clonal dynamics and genetic factors play a crucial role in the prevalence of macrolide-resistant isolates, beyond antibiotic consumption.